L16 - Anaesthetics Flashcards
Of what aspects do analgesics provide minute-to-minute activity of CNS activity?
- arousal: brain stem - reticular activating system
- awareness: thalamo-cortical integration of information
- pain sensation: spinal levels and higher
- muscle activity and motor control: spinal and higher
What are the four stages of anaesthesia?
stage 1: analgesia - subject conscious - decreased responsiveness to pain stage 2: excitement - subject loses consciousness - may respond reflexively to pain (exaggerated reflexes) stage 3: surgical anaesthesia - regular respiration and spontaneous movements stop - some reflexes may still be intact stage 4: medullary paralysis - respiration and spontaneous movement may still be present - usually followed by coma and death
How does water solubility affect the delivery of anaesthetics?
- low water solubility gases = fast delivery to CNS lipids (brain)
because quickly saturate the blood stream and must be delivered to tissue to make space for the gas that the patient is still breathing in - high water solubility gas -= slow delivery to CNS lipids
What are the factors that affect the kinetics of anaesthesia?
- water solubility
low water solubility = fast delivery to CNS lipids
high water solubility = slow delivery to CNS lipids - rate of ventilation
increased rate of breathing = more efficient gas delivery - partial pressure of the gas
increased concentration of gas = increased delivery - cardiac output
higher HR = increased CO = increased delivery to brain
How is anaesthesia maintained?
- once induction of anaesthesia is achieved, gaseous anaesthetics delivered on minute-to-minute basis at MAC (minimum alveolar concentration)
- the more lipid-soluble the more potent = lower MAC
- some gases act in synergy so can maintain by simultaneous administration of 2 drugs below their MAC
What is MAC?
Minimum Alveolar Concentration
- measure of anaesthetic potency
- the concentration of gas needed to eliminate reflex movements in 50% of patients
What is the mechanism of action for gaseous anaesthetics?
- could potentially disrupt the lipid bilayer
What are some gaseous anaesthetics?
- halothane
- nitrous oxide
- enflurane
- isoflurane
What is the benefits of IV anaesthetics?
- can be used to push patient’s past stage 2 of anaesthesia
- injected so immediately high levels of drug in the blood stream which drops off in minutes as it goes to the brain
- patient unconscious in minutes
- drug also leaves brain in minutes but now administering gaseous anaesthetic
What are 2 types of IV anaesthetic?
- barbiturates e.g. thiopental (most common)
- ketamines
What are the benefits of barbiturates?
- highly lipid soluble
- ultra-fast acting and ultra-short duration
What are the adverse cardiovascular effects of barbiturates?
- reduced CO
- hypotension
- respiratory depression
- reduced cerebral blood flow and O2 utilisation
What is the effect of ketamines?
“dissociative anaesthetics”
- pain information to thalamus not processed by the patient
- patient appears to be awake but is actually unconscious
- amnesia, analgesia, rigidity or catatonia
- disorientations and hallucinations common
- very lipid soluble for fast but short acting
How are injected anaesthetic agents used?
- most commonly for induction of anaesthesia
- followed by gaseous anaesthetic
How are local anaesthetics different to gaseous and injected anaesthetics?
- do not produce a loss of consciousness
What are the main problems with cocaine?
acute toxicity and dependence
- is a monoamine reuptake inhibitor but also local anaesthetic so causes noradrenaline, dopamine and serotonin accumulation in extracellular space
Why is lignocaine beneficial compared to cocaine?
- is not a monoamine reuptake inhibitor
What are the features of an ideal local anaesthetic?
- selective blockage of sensation
- rapid onset and rapid reversibility (washout)
- reasonable duration of action
- non-toxic (locally and systemically)
What are the most commonly used local anaesthetics?
- lignocaine
- bupivacaine (longer acting)
What is the chemistry of local anaesthetics?
- most LAs are weak bases
- ionised form cannot cross cell membrane
- pH of blood and ECF is ~7.4 so ionised form predominates
What is the mechanism of action for LAs?
- sodium channel blockers (VSSC)
- block VSSCs from the inside of the axon so must get inside the cell first
- small diameter pain fibres are the most sensitive because they have little/no myelin so drug can easily get inside the axon
- “use dependence” = channel must be in open state for drug to get into channel i.e. must be some VSCC activity
- blocks AP so no depolarisation = no pain pathway
What are the short acting local anaesthetics? How long do they act for?
- benzocaine
- procaine
act for 30-60 minutes
What are the properties of benzocaine?
- topical
- non-toxic
- very low potency
What are the properties of procaine?
- infiltration
- least toxic
- slow onset
- potency = 0.5 (relative to lignocaine)
What are the intermediate duration local anaesthetics?
- lignocaine
- prilocaine
What are the properties of lignocaine?
- infiltration, nerve block, epidural, IV
- cardiotoxic
- rapid onset
What are the properties of prilocaine?
- infiltration, nerve block, epidural, IV
- less toxic
- potency = 1.0 (same as lignocaine)
- methaemoglobin (causes reduced affinity for oxygen in the blood)
What are the long duration local anaesthetics?
- bupivacaine
- amethocaine
What are the properties of bupivacaine?
- infiltration, nerve block, epidural
- cardiotoxic
- slow onset
- potency = 4 (cf. lignocaine)
What are the properties of amethocaine?
- spinal, topical
- slow onset
- potency = 5 (cf. lignocaine)
- systemic toxicity
What are the indications and contraindications of LA administration?
indications: - surgery when consciousness is required - widely used during "minor" procedures contraindications: - extensive surgical procedures due to risk of high dose LA toxicity - allergies or hypersensitivities to LAs - local inflammation at injection site - infections - ischaemia at injection site
precautions with paediatric, elderly or pregnant parties
Most LAs produce local vasodilation: how?
- direct action on blood vessels - by blocking VSSCs and causing smooth muscle relaxation
- direction action on sympathetic nerves - by blocking VSSCs and preventing NA release
vaodilation causes rapid absorption of the LA - washout of the tissues (if absorption exceeds elimination = toxicity)
How is the undesirable vasodilation effect of LAs counteracted?
- LAs often delivered with vasoconstrictors (e.g. adrenaline, felypressin)
this prolongs the LAs duration of action, and decreases the risk of systemic toxicity
vasoconstrictors not used for nerve blocks where end arteries exist e.g. fingers, toes, ears, nose due to risk of ischaemia and gangrene
